Assessment and Treatment of Post Patent Ductus Arteriosus Ligation Syndrome Afif F. EL-Khuffash, MD, DCE, FRCPI1, Amish Jain, MD2,3,4, Dany Weisz, MD5, Luc Mertens, MD6, and Patrick J. McNamara, MD, MRCPCH3,4,7,8 Objective To compare differences in tissue Doppler imaging, global longitudinal strain (GLS), and cardiac troponin T (cTnT) between infants with low (200 mL/kg/min) left ventricular (LV) output 1 hour after duct ligation and assess the impact of milrinone treatment on cardiac output and myocardial performance. Study design LV function was assessed preoperatively and 1 and 18 hours postoperatively. Infants were categorized into a low-output or a normal-output group based on the echocardiographic assessment of LV output at 1 hour. Results Thirty infants with a mean gestation of 25.3 weeks were enrolled. LV basal lateral S0 , basal septal S0 , and basal right ventricular S0 were lower in the low-output group (n = 19) at 1 hour postoperatively, with no significant difference in GLS (low-output 10.3% vs high-output 14.4%, P >.05) or cTnT between the groups. Patients in the low-output group were treated with milrinone, and by 18 hours LV performance recovered to levels comparable with the high output group. cTnT values increased at 18 hours in the whole cohort with no significant difference between the groups. Conclusion Tissue Doppler imaging and GLS provide novel insights and further characterization of myocardial performance immediately after patent ductus arteriosus ligation. A reduction in tissue Doppler-derived LV systolic velocity may further help in monitoring cardiac performance after patent ductus arteriosus ligation and for monitoring the effects of treatment. (J Pediatr 2014;-:---).
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he decision to undergo patent ductus arteriosus (PDA) ligation is subject to much debate and controversy, in part related to the high morbidity in survivors less than 1000 g.1 Postligation cardiac syndrome (PLCS) complicates the postoperative course in 40%-50% of preterm infants. PLCS is a clinical entity characterized by hypotension requiring inotropic support, and/or ventilation/oxygenation failure, usually occurring 6-12 hours after ligation.2,3 Several studies have investigated the physiologic mechanisms contributing to cardiorespiratory instability after PDA ligation and demonstrated a decrease in shortening fraction and ejection fraction associated with an increase in systemic vascular resistance (SVR) and a sudden reduction in preload.2,4 The sudden increase in SVR is not well tolerated by the preterm myocardium.3,5 Our group recently demonstrated that a left ventricular output (LVO) 200 mL/min/kg) vs low (
T
he decision to undergo patent ductus arteriosus (PDA) ligation is subject to much debate and controversy, in part related to the high morbidity in survivors less than 1000 g.1 Postligation cardiac syndrome (PLCS) complicates the postoperative course in 40%-50% of preterm infants. PLCS is a clinical entity characterized by hypotension requiring inotropic support, and/or ventilation/oxygenation failure, usually occurring 6-12 hours after ligation.2,3 Several studies have investigated the physiologic mechanisms contributing to cardiorespiratory instability after PDA ligation and demonstrated a decrease in shortening fraction and ejection fraction associated with an increase in systemic vascular resistance (SVR) and a sudden reduction in preload.2,4 The sudden increase in SVR is not well tolerated by the preterm myocardium.3,5 Our group recently demonstrated that a left ventricular output (LVO) 200 mL/min/kg) vs low (
